Telemedicine in Neurology: Challenges and Opportunities.

Objective: Our objective is to explore challenges encountered by neurologists with the use of telemedicine in neurology. Methods: A cross- sectional study via an anonymous survey to explore neurologists' experiences with telemedicine. They survey was sent to randomly selected 200 participants from Academic Institutions in the United States. Descriptive statistics were reported as percentages for each survey question. Results: 110 neurologists completed the survey. Fifty-one percent of neurologists stated that they experienced technological issues in (1%-20%) of telemedicine visits and 57% of neurologists needed technological assistance from informational technology support. With regards to the impact of limited neurological examination via telemedicine, 34% of neurologists agreed that the limited examination makes them worried that they are providing a suboptimal care to patients and 55% recommended a subsequent in-person visit (in 1%-20% of telemedicine visits) for further evaluation. Among the challenges that hindered patients' ability to participate in telemedicine visits, 95% of neurologists rated patients' technological challenges with setting up telemedicine to be the most common issue encountered, 37% of neurologists rated patient's cognitive/mental disability to be the second most common challenge to complete telemedicine visits as well as availability of interpreter services for non-English speaking patients. Neurologists rated improving administrative support (39%), integration of EMR for video and telephone calls (37%), and sufficient time allotment to complete telemedicine visits (27%) to be the most important issues to address to optimize the use of telemedicine in neurology. Significance: Potential opportunities to improve neurologists' experiences in telemedicine include improving technological support, integration of virtual platforms within the EMR, and adequate administrative support. Patients with cognitive/physical disabilities may need additional support to engage in the health system via telemedicine.

Egr1 mediates the effect of insulin on leptin transcription in adipocytes.

In mammals, leptin production in adipocytes is up-regulated by feeding and insulin. Although this regulatory connection is central to all physiological effects of leptin, its molecular mechanism remains unknown. Here, we show that the transcription factor early growth response 1, Egr1, is rapidly but transiently induced by insulin in adipose cells both in vitro and in vivo, and its induction is followed by an increase in leptin transcription. ChIP and luciferase assays demonstrate that Egr1 directly binds to and activates the leptin promoter. Interestingly, the lipid droplet protein FSP27 may work as a co-factor for Egr1 in regulating leptin expression. By using siRNA-mediated knockout of Egr1 along with its overexpression in adipocytes, we demonstrate that Egr1 is both necessary and sufficient for the stimulatory effect of insulin on leptin transcription.

Transcription factor and microRNA interactions in lung cells: an inhibitory link between NK2 homeobox 1, miR-200c and the developmental and oncogenic factors Nfib and Myb.

BACKGROUND: The transcription factor NK2 homeobox 1 (Nkx2-1) plays essential roles in epithelial cell proliferation and differentiation in mouse and human lung development and tumorigenesis. A better understanding of genes and pathways downstream of Nkx2-1 will clarify the multiple roles of this critical lung factor. Nkx2-1 regulates directly or indirectly numerous protein-coding genes; however, there is a paucity of information about Nkx2-1-regulated microRNAs (miRNAs). METHODS AND RESULTS: By miRNA array analyses of mouse epithelial cell lines in which endogenous Nkx2-1 was knocked-down, we revealed that 29 miRNAs were negatively regulated including miR-200c, and 39 miRNAs were positively regulated by Nkx2-1 including miR-1195. Mouse lungs lacking functional phosphorylated Nkx2-1 showed increased expression of miR-200c and alterations in the expression of other top regulated miRNAs. Moreover, chromatin immunoprecipitation assays showed binding of NKX2-1 protein to regulatory regions of these miRNAs. Promoter reporter assays indicated that 1kb of the miR-200c 5' flanking region was transcriptionally active but did not mediate Nkx2-1- repression of miR-200c expression. 3'UTR reporter assays support a direct regulation of the predicted targets Nfib and Myb by miR-200c. CONCLUSIONS: These studies suggest that Nkx2-1 controls the expression of specific miRNAs in lung epithelial cells. In particular, we identified a regulatory link between Nkx2-1, the known tumor suppressor miR-200c, and the developmental and oncogenic transcription factors Nfib and Myb, adding new players to the regulatory mechanisms driven by Nkx2-1 in lung epithelial cells that may have implications in lung development and tumorigenesis.